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作 者:胡丽红[1] 刘冰熔[1] 刘丹[1] 关景明[1] 吕志武[1] 杜雅菊[1]
机构地区:[1]哈尔滨医科大学附属第二医院消化科,黑龙江省哈尔滨市150086
出 处:《世界华人消化杂志》2006年第23期2270-2274,共5页World Chinese Journal of Digestology
基 金:黑龙江省攻关重点资助项目;No.GC02C148-01;2005年哈尔滨医科大学优秀研究生创新基金资助项目;No.HCXS2005015~~
摘 要:目的:研究重组腺病毒Ad-IκBαM对5-氟尿嘧啶(5-FU)诱导胃癌细胞凋亡的作用情况,进而研究胃癌细胞抵抗5-FU的机制.方法:培养胃癌SGC-7901细胞,感染重组腺病毒Ad-IκBαM的细胞为实验组,感染Ad- IκBα及非感染的空白对照为对照组,以5 mg/L 5-FU加入上述各组细胞,采用EMSA法检测5-FU处理后各组细胞内NF-κB激活情况:应用MTT和TUNEL法分别检测5-FU对各组细胞诱导凋亡的情况.结果:5-FU作用于胃癌细胞可使细胞内NF-κB激活,感染Ad-IκBαM使NF-κB活性受到明显抑制.MTT法证明,5-FU作用后,感染Ad-IκBαM细胞的凋亡(56.36%±0.60%)较感染Ad-IκBα组(47.50%±1.42%)及未感染组(42.95%±1.27%)明显,各组间比较有统计学差异(P≤0.001);TUNEL法结果与MTT相符,感染Ad-IκBαM组的凋亡率为29.7%±2.5%,明显高于感染Ad-IκBα组(20.0%±2.6%)及未感染组(12.3%±1.1%)(P<0.01).可见,感染Ad- IκBαM可明显提高5-FU诱导的细胞凋亡.结论:感染Ad-IκBαM可通过抑制胃癌细胞NF-κB的活性增强5-FU的诱导凋亡作用.AIM: To investigate the role of recombinant adenovirus IkBαM (Ad-IkBαM) on the apoptosis of gastric carcinoma SGC-7901 cells induced by 5-fluorouracil (5-FU) as well as the possible mechanism. METHODS: The cultured SGC-7901 cells were divided into group A, B and C. The cells in group A and B were infected with Ad-IkBαM and Ad-IkBα, respectively, and those in group C served as controls. 5-FU was added to each group at the concentration of 5 mg/L, respectively. Electrophoretic mobility shift assays were used to detect the activation of nuclear facter kappa B (NF-kB) in all the groups, and the 5-FUinduced apoptosis of SGC-7901 cells was tested by MTT and TUNEL method. RESULTS: After 5-FU treatment, NF-kB was activated in gastric carcinoma cells, but in the cells infected with Ad-hcBαM, the activity of NF- kB was inhibited. MTT assay indicated that the apoptosis rate of cells infected with Ad-IkBαM (56.36% ± 0.60%) was significantly higher than that of cells infected with Ad-hcBα (47.50% ± 1.42%), or without infection (42.95% ± 1.27%) (P 〈 0.001). TUNEL method showed that the apoptosis rate was 29.7% ± 2.5% in the cells infected with Ad-hcBαM, which was also significantly higher than that of cells infected with Ad-hcBα (20.0% ± 2.6%) or without infection (12.3% ±1.1%) (P 〈 0.01). Therefore, infection with Ad-IkBαM markedly promoted the apoptosis induced by 5-FU. CONCLUSION: Infection with Ad-IkBαM can effectively inhibit the activation of NF-kB in human SGC-7901 cells, and increase the apoptosis induced by 5-FU.
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